We have:(a) demonstrated that Clara cell 10kDa (cc10kDa) protein is the counterpart of rabbit uteroglobin (rUG) by obtaining over expression of recombinant cc10kDa in E.coli and detailed characterization of this protein; (b) established that human UG (hUG) gene is expressed in many organs and tissues besides the pulmonary Clara cells suggesting that hUG may be a multifunctional cytokine-like protein; (c) delineated that hUG gene expression in the human endometrium is regulated by ovarian steroid hormones; (d) established and characterized two temperature-sensitive epithelial cell lines derived from the rabbit endometrium which differentiate in vitro and express UG gene in response to steroid hormones; (e) developed a highly improved expression vector which stabilizes the cDNA to be expressed in a bacterial host and requires no ampicillin for this stability; (f) crystallized recombinant hUG and carried out X-ray diffraction studies; (g) carried out multidimensional NMR studies on hUG which suggest a structure for this protein which is nearly identical to rUG; (h) site-directed mutagenesis of hUG suggests that mutation of Lys-43-> Asp 43 leads to inactivation of phospholipase A2-inhibitory property of hUG; (i) discovered a novel high affinity cell surface binding protein for hUG on NIH 3T3 and human trophoblast cells and when huG binds to this putative receptor it inhibits chemoinvasion of the artifiicial basement membrane by these cells. In addition, the choriocarcinoma cells were found to be lacking this receptor and their invasion is not affected by hUG; (j) established that invasion of prostatic carcinoma cells is suppressed by hUG; (k) identified a specific region of group I PLA2(residues 21-40) interaction of which with a neutralizing antibody leads to complete inhibition of its activity; (l) filed an invention report on the anti-invasive effects of hUG (m) established and standardized a radiometric assay for HIV-1 protease;(n) completed a preliminary study on the beneficial effects of hUG on a primate model of neonatal respiratory distress syndrome. The results suggest that recombinant hUG inhibits lung PLA2 activity and prevents migration of inflammatory cells into this organ. Long-term effects of this therapy are now being investigated (o) established that osteopontin (OP)-fibronectin interaction in bone and extracellular matrix (ECM) protein is mediated by transglutaminase (TG) and (p) demonstrated that disruption of cellular Src (c-Src) protooncogene causes dramatic suppression of OP gene expression. Since OP is essential for new bone formation by ostcoclas, our results may in part explain.